Course # 30992 • Acute Coronary Syndrome: An Overview for Nurses


Study Points

  1. Explain the pathophysiology of ACS, including the role of plaque formation and rupture.
  2. Discuss risk factors and key aspects of screening for atherosclerotic plaque and coronary heart disease (CHD).
  3. Describe components of triaging patients with suspected ACS.
  4. Identify key elements that should be included in the history and physical examination of patients with suspected ACS, including the role of stress tests.
  5. List key elements to include in chest pain assessment for a patient with possible ACS.
  6. Outline the role of 12-lead ECG and cardiac biomarkers in the diagnosis and risk stratification of ACS.
  7. Review key recommendations for the medical and nursing management of patients with UA/NSTEMI, including initial treatment, early inpatient care, and recommended pharmacotherapy.
  8. Describe ischemia-guided and invasive strategies related to the management of patients with UA/NSTEMI.
  9. Discuss key components of medical and nursing management of patients with variant angina and cocaine-induced ACS.
  10. Explain the role of PCI in the management of STEMI, including the issues of timing, stent selection, supporting pharmacologic therapy, risks, and possible complications.
  11. Outline the use of fibrinolytic therapy as a reper­fusion therapy in the management of STEMI, including the issues of indications, contraindications, supporting pharmacologic therapy, and risks.
  12. List key measures used to prevent reocclusion in coronary circulation following reperfusion with PCI or fibrinolytic therapy.
  13. Discuss the role of smoking cessation in reducing the risk of recurrent ACS and tools for helping patients quit smoking.
  14. Describe other measures patients may take to reduce risk of recurrent ACS and ongoing CHD from hypertension, dyslipidemia, and other modifiable risk factors.
  15. Explain factors that impact a patient's adherence to prescribed therapy and measures to reduce risk of recurrent coronary disease.

    1 . The initial, precipitating event thought to trigger formation of atherosclerotic plaque in a coronary artery is
    A) hypotension.
    B) a genetic trait.
    C) arterial stenosis.
    D) injury to the artery endothelium.

    PATHOPHYSIOLOGY OF ACS

    The underlying cause of ACS is a form of atherosclerosis known as CHD. In CHD, lipids, calcium, fibrin, and other cellular substances/cellular debris are deposited in the lining of the arteries, forming atherosclerotic plaques at sites with low-velocity blood flow (e.g., branch points, inner curvatures) [30]. Although the exact mechanisms are not completely understood, most researchers agree that injury to the inner (endothelial) layer of the artery initiates a series of biochemical events that result in the formation of atherosclerotic plaque. High levels of low-density lipoprotein (LDL) alone can cause atherosclerosis; however, it is most often the case that lower levels of LDL combined with other identified risk factors, including cigarette smoke, low levels of high-density lipoprotein (HDL), hypertension, diabetes, male sex, and family history, lead to atherosclerosis [30]. Individuals with very low LDL typically do not develop clinically significant atherosclerotic plaques, even in the presence of these risk factors.

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    2 . Stimuli for plaque erosion resulting in thrombus formation include
    A) sodium deficiency.
    B) elevated hemoglobin.
    C) high levels of HDL in the bloodstream.
    D) high levels of LDL in the bloodstream and cigarette smoking.

    PATHOPHYSIOLOGY OF ACS

    Formation of a thrombus occurs when the fibrous cap of an atherosclerotic lesion erodes or ruptures, exposing the red cell-rich lipid core to circulating blood. It is thought that the same stimuli that are responsible for the initial injury to the vessel wall are also responsible for causing erosion or rupture of vulnerable plaque (i.e., inflammation). Cigarette smoking and high levels of circulating LDL head the list of injurious agents along with hypertension and diabetes [1,30,31,32,33].

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    3 . Irreversible cardiac tissue death occurs after how many minutes of ischemia?
    A) 10 seconds
    B) 1 minute
    C) 20 minutes
    D) 2 hours

    PATHOPHYSIOLOGY OF ACS

    When a thrombus occludes a coronary artery, oxygen supply to the area of the heart supplied by that vessel is reduced. When the supply becomes insufficient to meet the tissue's metabolic demands, the myocardial cells become ischemic; ischemia can develop within 10 seconds. After 1 minute of inadequate oxygen supply, the heart's function is affected. Irreversible tissue death and damage will occur after 20 minutes of ischemia [33].

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    4 . The Framingham Risk Score underestimates CHD risk in which of the following populations?
    A) Younger individuals
    B) White middle-aged men
    C) White middle-aged women
    D) Older black and white individuals, particularly women

    RISK FACTORS FOR CHD

    The Framingham Heart Study identified the first risk factors, and these factors were integrated into a risk-assessment tool, the Framingham Risk Score [49]. The factors in the Framingham Risk Score include age, total cholesterol level, HDL level, systolic blood pressure, treatment for hypertension, and cigarette smoking, and the score is used to determine the 10-year risk of so-called hard CHD (defined as MI or coronary-related death) among asymptomatic adults. The Framingham risk score is one of several scores that involve several traditional risk factors for assessing risk; other scores recommended include the Systematic Coronary Risk Evaluation (SCORE), PROCAM (men) and Reynolds (separate scores for men and women) [50]. The use of one of these risk calculators is a class IB recommendation from the American College of Cardiology Foundation and American Heart Association [50]. It is important to consider the populations on which these risk scores are based. For example, the Framingham Risk Score was developed on the basis of risk factors identified in the Framingham Heart Study, which involved a primarily white, middle-aged population. When the risk score has been evaluated in other populations, it has been found to underestimate the risk of CHD among older (mean age: 73.5 years) black and white individuals, especially women [51]. ACC/AHA guidelines published in 2013 recommend that race- and sex-specific Pooled Cohort Equations be used to predict 10-year risk of a first hard atherosclerotic cardiovascular disease event in non-Hispanic black and non-Hispanic white individuals (class IB) [52]. These equations were developed on the basis of data on participants from several large racially and geographically diverse studies [52]. The guidelines also note that the sex-specific pooled cohort equations for non-Hispanic white individuals may be considered to estimate risk for people other than black and non-Hispanic white individuals (class IB) [52].

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    5 . Evaluating which of the following nontraditional risk factors for CHD is recommended in asymptomatic adults?
    A) Genomic testing
    B) Natriuretic peptides
    C) Family history of atherothrombotic CHD
    D) Brachial/peripheral flow-mediated dilation

    RISK FACTORS FOR CHD

    EVIDENCE-BASED RECOMMENDATIONS FOR USE OF NONTRADITIONAL RISK FACTORS TO EVALUATE CHD RISK IN ASYMPTOMATIC ADULTS

    Nontraditional Risk FactorRecommendation (Class, Level of Evidence)
    Family history of CHD
    Recommended for all asymptomatic women (IB)
    May be considered if risk-based treatment decision is uncertain after quantitative risk assessment (IIbB)a
    Family history of atherothrombotic CHDRecommended for all asymptomatic adults (IB)
    Genomic testingNot recommended (IIIB)
    Lipoprotein and apolipoprotein assessmentsNot recommended (IIIC)
    Natriuretic peptidesNot recommended (IIIB)
    C-reactive protein
    May be considered if a risk-based treatment decision is uncertain (after quantitative risk assessment IIbB)a
    Not recommended for asymptomatic adults at high risk (IIIB)
    May be reasonable for asymptomatic men (50 years of age or younger) or women (60 years of age or younger) who are at intermediate risk (IIbB)
    Hemoglobin A1C
    May be reasonable for risk assessment in asymptomatic adults who do not have diabetes (IIbB)
    May be considered for asymptomatic adults with diabetes (IIbB)
    Testing for microalbuminuria
    Utility is uncertaina
    Reasonable for asymptomatic adults with hypertension or diabetes (IIaB)
    Might be reasonable for asymptomatic adults at intermediate risk who do not have hypertension or diabetes (IIbB)
    Lipoprotein-associated phospholipase A2Might be reasonable for asymptomatic adults at intermediate risk (IIbB)
    Resting electrocardiography (ECG)
    Reasonable for asymptomatic adults with hypertension or diabetes (IIaC)
    May be considered for asymptomatic adults who do not have hypertension or diabetes (IIbC)
    Transthoracic echocardiography (to detect left ventricular hypertrophy)
    May be considered for asymptomatic adults who have hypertension (IIbB)
    Not recommended for asymptomatic adults who do not have hypertension (IIIC)
    Measurement of carotid intima-media thickness
    Not recommended (IIIB)a
    Reasonable for asymptomatic adults at intermediate risk (IIaB)b
    Brachial/peripheral flow-mediated dilationNot recommended (IIIB)
    Measurement of arterial stiffnessNot recommended outside of research settings (IIIC)
    Measurement of ankle-brachial index
    May be considered if a risk-based treatment decision is uncertain after quantitative risk assessment (IIbB)a
    Reasonable for asymptomatic adults at intermediate risk (IIaB)
    Exercise ECGMay be considered for asymptomatic adults at intermediate risk (IIbB)c
    Stress echocardiographyNot indicated for asymptomatic adults at low or intermediate risk (IIIC)
    Stress myocardial perfusion imaging
    Not indicated for asymptomatic adults at low or intermediate risk (IIIC)
    May be considered for assessment of advanced cardiovascular risk in asymptomatic adults who have diabetes or asymptomatic adults with a strong family history of CHD or when previous risk assessment suggests high risk of CHD (IIbC)
    Coronary artery calcium scoring
    May be considered if a risk-based treatment decision is uncertain after quantitative risk assessment(IIbB)a
    Not recommended for persons at low risk (10-year risk <6%) (IIIB)
    Reasonable for asymptomatic adults at intermediate risk (10-year risk of 10% to 20%) (IIaB)
    Reasonable for asymptomatic adults (40 years and older) who have diabetes (IIaB)
    May be reasonable for persons at low to intermediate risk (10-year risk of 6% to 10%) (IIbB)
    Coronary computed tomography angiographyNot recommended for asymptomatic adults (IIIC)
    Magnetic resonance imaging of plaqueNot recommended for asymptomatic adults (IIIC)
    aRecommended in the 2014 guideline.
    bPublished recommendations on required equipment, technical approach, and operator training and experience for performance of the test must be carefully followed to achieve high-quality results.
    cMay also be considered for sedentary adults who plan to start a vigorous exercise program.
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    6 . Updated guidelines increasingly emphasize managing lifestyle risk factors for primary prevention of CHD, including
    A) obesity.
    B) poor diet.
    C) physical inactivity.
    D) All of the above

    RISK FACTORS FOR CHD

    Increased emphasis has been placed on better management of lifestyle habits as primary prevention of CHD. Lifestyle risk factors such as obesity, poor diet, and physical inactivity have a great influence on traditional risk factors such as blood pressure and cholesterol levels, as well as on novel risk factors, such as inflammation and endothelial function [78]. Lifestyle management is a key component of the new guidelines for the treatment of cholesterol levels and hypertension, and several other guidelines have addressed issues related to lifestyle behaviors, such as obesity, diet, and physical activity. The ACC/AHA/TOS (The Obesity Society) developed a guideline on the management of overweight and obesity, and some members of the Expert Panel authored a separate review on the evidence statements related to cardiovascular risk [79,80]. The AHA/ACC also published a guideline on lifestyle management to reduce cardiovascular risk in 2013 [81]. In its guideline of cardiac screening, the ACP notes that strategies to improvement lifestyle behaviors should be emphasized [65]. The USPSTF recommends counseling to promote a healthful diet and physical activity to prevent cardiovascular disease, and the AHA focuses on changing lifestyle behaviors in its guide for improving cardiovascular health at the community level [82,83,84]. The decision to offer or refer adults without cardiovascular risk factors to behavioral counseling should be individualized by the primary care provider [85].

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    7 . Which of the following is a primary goal of the initial evaluation of a patient with suspected ACS?
    A) To begin treatment
    B) To identify risk factors for ischemic stroke
    C) To estimate the short-term risk of adverse outcomes
    D) To determine the long-term goals and potential discharge plan

    TRIAGE

    The two primary goals of the initial evaluation in the emergency department are to determine the likelihood that an individual has ACS and to estimate the short-term risk of adverse outcome(s) [3]. The findings of the history, physical examination, ECG, and cardiac troponin levels have been integrated into risk assessment scores and clinical prediction algorithms to help identify patients at increased risk of adverse outcomes. Identifying patients at high risk is most important, as these patients will gain the greatest absolute benefit from appropriate therapy [2,3]. Because timely, appropriate treatment depends on results of the clinical findings and diagnostic testing, it is essential that this information is obtained as quickly as possible.

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    8 . Women with ACS are more likely than men to have
    A) normotension.
    B) hyperlipidemia.
    C) no history of diabetes.
    D) a history of angina or MI.

    DIAGNOSIS

    Research has shown that a history of traditional cardiac risk factors varies among some subgroups. Women with ACS are more likely than men to have a history of diabetes, hypertension, or hyperlipidemia [11,101,102,103,104,105,106]. (It has been suggested that this is due to the fact that women tend to develop ACS at an older age) [103,106]. Women are less likely to be smokers, to have a history of angina or MI, and to have had PCI or CABG, regardless of the cardiac history [104,107,108]. Data on the prevalence of risk factors across racial/ethnic subgroups with ACS was reported in 2008 (Table 6) [109].

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    9 . So-called "classic" chest pain associated with ACS is described as
    A) extreme hunger.
    B) a pricking feeling.
    C) sharp, stabbing pain in the chest.
    D) diffuse pain or pressure in the substernal or epigastric area.

    DIAGNOSIS

    Chest pain is the most commonly reported symptom in all patients with ACS, regardless of age, gender, race/ethnicity, or the presence of comorbid conditions [14,116,117]. So-called "classic" ACS-related chest pain has been described as diffuse pain or pressure in the substernal or epigastric area that frequently radiates to the neck, jaw, and left arm [22,101,118,119]. Chest pain related to ACS usually begins abruptly and lasts at least 15 to 20 minutes; however, the duration of pain varies among patients [101,120]. Pain that lasts for longer than 20 minutes is associated with increased short-term risk of MI (nonfatal or fatal) [121]. The intensity of "classic" ACS chest pain increases over time, reaching maximal intensity after a few minutes [101,122]. Pain is usually worse with activity and improves with rest [101].

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    10 . Which of the following is a potentially life-threatening cause of non-ACS chest pain?
    A) Pleurisy
    B) Panic attack
    C) Aortic dissection
    D) Gastroesophageal reflux

    DIAGNOSIS

    DIFFERENTIAL DIAGNOSIS OF CHEST PAIN

    Life-Threatening Causes
    Aortic dissection
    Pulmonary embolism
    Pneumothorax
    Expanding aortic aneurysm
    Other Causes
    Pneumonia
    Pleuritis
    Pericarditis
    Costochondritis
    Cervical disc disease
    Peptic ulcer disease
    Gastroesophageal reflux
    Biliary disease
    Pancreatitis
    Panic attack
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    11 . Which of the following chest pain locations is considered atypical in patients with ACS?
    A) Substernal
    B) Left-sided chest
    C) Between the shoulder blades
    D) None of the above

    DIAGNOSIS

    An increasing number of studies have demonstrated that atypical chest pain occurs more often in several subgroups of patients, especially women, older individuals, and people with diabetes [14,102,117,126,131,132,133,134]. In addition, the findings of several studies and literature reviews have demonstrated that women with ACS are more likely to have pain or discomfort in the jaw, neck, throat, arm/shoulder, and back [102,127,131]. Failure to recognize atypical symptoms of ACS has been found to delay diagnosis and/or result in the use of less aggressive treatment. It has been estimated that more than 40% of patients with angina have one or more "atypical" elements in their chest pain description [135,136]. Atypical symptoms that have been found to be associated with ACS include shortness of breath, fatigue, lethargy, indigestion, anxiety, tingling in upper extremities, palpitations, loss of appetite, and flushing. Words commonly used to describe "atypical" chest pain associated with ACS include numbness, tingling, burning, stabbing, or pricking. Atypical chest pain location includes any area other than substernal or left sided, such as the back, area between shoulder blades, upper abdomen, shoulders, elbows, axillae, and ears [135,136].

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    12 . On 12-lead ECG, the presence of a pathologic Q wave in the absence of ST-segment elevation and T-wave changes indicates
    A) an old infarct.
    B) acute STEMI.
    C) acute NSTEMI.
    D) congenital defects.

    DIAGNOSIS

    The first of the three classic signs is ST-segment elevation. It may be followed by T-wave inversion and pathologic Q-wave formation. This sequence of changes is called the electrocardiographic evolution of an infarction. Because these changes happen over a period of time, a series of 12-lead ECG tracings may be required for accurate diagnosis. In the very early stages of infarct, clear patterns may not be immediately revealed on ECG. As always, ECG findings should be correlated with clinical signs and symptoms. Over a period of months to days, ST-segment elevation and T-wave changes will resolve and no longer be present on 12-lead ECG recordings. Pathologic Q waves, on the other hand, frequently remain permanently. Presence of a pathologic Q wave on 12-lead ECG with no evidence of ST-segment elevation or T-wave changes usually indicates that the person has had an infarct in the past [1,33,47]. It is important to note that ST-segment and T-wave changes are not specific for ACS and may be the result of another disease or condition. Left ventricular aneurysm, pericarditis, myocarditis, Prinzmetal angina, Takotsubo cardiomyopathy, early repolarization, and Wolff-Parkinson-White syndrome may cause ST-segment elevation [3]. T-wave inversion can be caused by central nervous system events and treatment with tricyclic antidepressants or phenothiazines.

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    13 . ST-segment elevation in leads II, III, and aVF indicates
    A) lateral wall infarction.
    B) inferior wall infarction.
    C) anterior wall infarction.
    D) poor recording technique.

    DIAGNOSIS

    ECG CHANGES AND DIAGNOSIS OF STEMI

    Leads Showing ChangesLocation of InfarctionLocation of Occlusion
    II, III, aVFInferior wallRight coronary artery
    I, aVL, V5–6Lateral wallCircumflex artery
    V1–V4Anterior wallLeft anterior descending
    Reciprocal changes only in V1–V2, sometimes V4Suspect posterior wall of the heartRight coronary artery
    ST elevation in inferior leads and lead V1Suspect right ventricular wallRight coronary artery
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    14 . The recommended biomarker for detecting cardiac damage is
    A) CK-MB.
    B) creatine kinase.
    C) cardiac troponin.
    D) B-type natriuretic peptide (BNP).

    DIAGNOSIS

    Cardiac biomarkers are detectable intracellular macromolecules released into the circulation after cardiomyocyte injury and death. The biomarkers once used—creatinine kinase (CK)-MB and myoglobin—have been replaced by cardiac-specific troponin (troponin I or T) because of the latter's high concentration in myocardium, near-absolute specificity for myocardial tissue, their absence in the blood of healthy individuals, and their high clinical sensitivity [2,3,22]. Measurement of CK-MB or myoglobin levels was not useful or cost-effective [157].

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    15 . The initial drug of choice for relief of acute chest pain in all patients with suspected ACS is
    A) oral metoprolol 25 mg.
    B) sublingual nitroglycerin.
    C) continuous heparin infusion.
    D) sustained-release morphine tablets.

    TREATMENT OF UA/NSTEMI

    ADJUNCTIVE TREATMENT INDICATIONS FOR PATIENTS WITH UA/NSTEMI OR STEMI

    Adjunctive TherapyUA/NSTEMISTEMIComments
    Analgesia
    NitroglycerinAll patients, unless contraindicated (class IC)No recommendationContraindicated for patients with hypotension or who have used sildenafil or vardenafil within previous 24 hrs or tadalafil within previous 48 hrs (class IIIB).
    All patients, unless contraindicated (class IB)No recommendation
    MorphineReasonable for patients who have chest pain unrelieved by maximally tolerated anti-ischemic medications (class IIbB)
    Not specifically recommended.
    Narcotics should be considered if high-dose aspirin fails to relieve pain (class IIbC)
    Anti-Ischemia Therapy
    Beta blocker
    All patients, unless contraindicated (class IA)
    Continue during and after hospitalization, unless contraindicated (class IC)
    Re-evaluate patients with initial contraindications to beta blockers for subsequent use (class IC)
    All patients, unless contraindicated (class IB)
    Continue during and after hospitalization, unless contraindicated (class IB)
    Re-evaluate patients with initial contraindications to beta blockers for subsequent use (class IC)
    Administer in the first 24 hours.
    Contraindicated for patients with signs of heart failure, evidence of low-output state, increased risk of cardiogenic shock, or other contraindications to beta blockers.
    ACE inhibitorStarted and continued in all patients with left ventricular ejection fraction less than 40% and in patients with hypertension, diabetes, or stable CKD, unless contraindicated (class IA)All patients (within the first 24 hours) with anterior location, HF, or ejection fraction less than or equal to 0.40, unless contraindicated (class IA)
    Contraindicated for patients with hypotension (systolic blood pressure of <100 mm Hg or <30 mm Hg below baseline).
    An angiotensin receptor blocker should be used for patients intolerant of ACE inhibitors.
    Calcium-channel blockerPatients with continued or recurrent ischemia or with contraindications to beta blockers (class IB)No recommendation
    Antiplatelet Therapy
    Aspirin (non-enteric coated, chewable)
    All patients (class IA)
    Continued indefinitely
    All patients (class IA)
    Continued indefinitely
    Should be given as soon as possible at time of evaluation.
    Contraindicated for patients who have aspirin allergy or active bleeding
    Lower dose is reasonable during initial period post-stent implantation in patients at risk of bleeding.
    Consider clopidogrel or warfarin if aspirin is contraindicated. Monitor closely.
    Clopidogrel
    All patients (class IB)
    Administer to patients who are unable to take aspirin (class IB)
    Maintenance dose daily, continued preferably for up to 1 year (class IB)
    All patients (in addition to aspirin), before or at the time of PCI, if not already started and who are undergoing PCI within 24 hours of receiving fibrinolytic therapy (class IC)
    Daily dose should be continued for 1 year (class IC)
    Loading dose not recommended for older (>75 years of age) patients with STEMI. Should be withheld for 5 days in patients to have CABG (class IB). Monitor closely when used in conjunction with warfarin.
    Prasugrel
    Not recommended for initial platelet therapy.
    All patients undergoing PCI with stenting should be given a loading dose and at least 1 year of maintenance therapy with this or other P2Y inhibitor if not given clopidogrel (class IB).
    All patients undergoing PCI with stenting should be given a loading dose and at least 1 year of maintenance therapy with this or other P2Y inhibitor if not given clopidogrel (class IB).
    Should not be given sooner than 24 hours after administration of a fibrin-specific agent or 48 hours after administration of a non-fibrin-specific agent (class IIaB)
    Should be withheld for at least 7 days in patients to have CABG (class IB)
    Should not be administered to patients with history stroke or transient ischemic attack (class IIIB)
    TicagrelorAll patients undergoing PCI with stenting should be given a loading dose and at least 1 year of maintenance therapy with this or other P2Y inhibitor if not given clopidogrel (class IB).All patients (in addition to aspirin) undergoing PCI with stenting should be given a loading dose and at least 1 year of maintenance therapy with this or other P2Y inhibitor if not given clopidogrel (class IB).
    Should be withheld for at least 5 days in patients to have CABG (class IB)
    May only be used with lower doses (81 mg) of aspirin
    Requires twice daily administration.
    Glycoprotein IIb/IIIa inhibitorPatients selected for early invasive treatment, along with dual-antiplatelet therapy, who are at intermediate or high risk (high troponin levels) (class IIbB)
    Reasonable for selected patients who are receiving unfractionated heparin to have abciximab with primary PCI (class IIaA); eptifibatide or tirofiban may also be considered with primary PCI (class IIaB)
    May be reasonable to administer in emergency department to patients selected for primary PCI (class IIbB)
    The rate of IV infusion of eptifibatide or tirofiban should be reduced by 50% for patients with estimated creatinine clearance <50 mgL/min
    Eptifibatide or tirofiban should be discontinued 2 to 4 hours before CABG (class IB)
    Anticoagulant Therapy
    Unfractionated heparin (UFH)
    Option for patients selected for early invasive treatment (class IB) and early conservative treatment (class IB)
    Dose adjusted according to hospital protocol to maintain therapeutic anticoagulation for 48 hrs or until PCI (class IB)
    Option for patients selected for primary PCI (class IC) or fibrinolytic therapy (class IC); administer for at least 48 hrs or until revascularization
    The UFH dose should be reduced when a glycoprotein IIb/IIIa inhibitor is also given (class IC)
    For patients undergoing PCI after receiving anticoagulant regimen, administer additional boluses of UFH as needed to support procedure (class IC)
    EnoxaparinOption for patients selected for early invasive treatment (class IA) and early conservative treatment (class IA)Option for patients selected for fibrinolytic therapy (class IA); administer for at least 48 hours; for use up to 8 days or until revascularization
    Discontinue enoxaparin 12 to 24 hrs before CABG (class IB)
    Reduce dose for creatinine clearance less than 30 mL/ min and/or ≥75 yrs of age
    BivalirudinOption for patients selected for early invasive treatment (class IB)
    Preferred over UFH with glycoprotein IIb/IIIa inhibitor in patients selected for PCI at high risk of bleeding (class IIaB)
    Useful supportive measure for primary PCI with/without prior treatment with UFH (class IB)
    Reduce dose for creatinine clearance less than 30 mL/min
    Discontinue bivalirudin 3 hrs before CABG (class IB)
    FondaparinuxOption for patients selected for early invasive treatment (class IB) and early conservative treatment (IB)Option for patients selected for fibrinolytic therapy (class IB)
    Should not be used as sole anticoagulant to support PCI in patients with NSTE-ACS due to an increased risk of catheter thrombosis
    Avoid for creatinine clearance less than 30 mL/min
    Discontinue 24 hrs before CABG.
    ACE = angiotensin-converting enzyme; CABG = coronary artery bypass graft; CKD = chronic kidney disease; HF = heart failure; PCI = percutaneous coronary intervention.
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    16 . Beta blockers act to
    A) reduce pain perception.
    B) dissolve the thrombus through fibrin degradation.
    C) decrease cardiac work and myocardial oxygen demand.
    D) increase heart rate and blood pressure in ischemic tissue.

    TREATMENT OF UA/NSTEMI

    The inhibition of beta-1 adrenergic receptors by beta blockers acts to decrease cardiac work and myocardial oxygen demand. Beta blockers also slow the heart rate, which helps enhance coronary blood flow. A beta blocker should be given orally to all ACS patients (unless contraindicated) within 24 hours of presentation [3]. This use of beta blocker therapy has been associated with significantly lower in-hospital mortality [173]. Contraindications include signs of heart failure, low-output state, increased risk of cardiogenic shock, or other relative contraindications to beta blockade.

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    17 . A common, often fatiguing side effect of ACE inhibitors is
    A) flushing.
    B) constipation.
    C) disseminated rash.
    D) a dry, nagging cough.

    TREATMENT OF UA/NSTEMI

    When administering ACE inhibitors, the following nursing actions should be taken [172]:

    • Monitor blood pressure for hypotension. Be alert for orthostatic hypotension and syncope.

    • Implement fall precautions as indicated by patient status.

    • Monitor serum potassium levels and renal function studies; elevated serum potassium levels or increasing signs of renal insufficiency/failure can be an indication that the medication should be discontinued.

    • Monitor for the development of intolerable side effects. A common and often fatiguing side effect is a dry, nagging cough.

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    18 . According to the ACC/AHA guideline, chewable aspirin should be given
    A) never.
    B) only to men.
    C) only after definitive diagnosis of ACS.
    D) to all individuals with no contraindications as soon as possible after arrival in the emergency department.

    TREATMENT OF UA/NSTEMI

    The ACC/AHA guideline recommends that aspirin be given as soon as possible after a patient arrives in the emergency department and continued indefinitely in patients who tolerate it [3]. However, adherence by emergency medical personnel to guidelines recommending prompt prehospital aspirin administration is only 45% [177]. Aspirin is contraindicated for patients who are allergic to the drug or who have active bleeding; clopidogrel is recommended for patients who cannot tolerate aspirin [3]. Aspirin should be nonenteric-coated and chewable, and the recommended dose is 162–325 mg. A maintenance dose of aspirin should be continued indefinitely, at a daily dose of 81–325 mg. Adherence to the recommended use of aspirin has been better than for other drug therapies for patients with UA/NSTEMI, with rates of 97% to 99% [10,140]. Rates of aspirin use have been reported to be lower for older individuals and women, especially women younger than 55 years of age [18,178].

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    19 . For patients with NSTE-ACS, enoxaparin is administered
    A) intravenously.
    B) subcutaneously.
    C) intramuscularly.
    D) by continuous infusion.

    TREATMENT OF UA/NSTEMI

    The ACC/AHA guideline recommends enoxaparin as an option for all patients with NSTE-ACS [3]. The recommended dose is 1 mg/kg, given subcutaneously, every 12 hours, and the drug is continued throughout the hospitalization or until PCI is done [3]. The dose should be decreased to 1 mg/kg daily for patients with a creatinine clearance less than 30 mL/min.

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    20 . The objective of an ischemia-guided strategy in the management of NSTEMI is to
    A) increase the volume of PCIs at participating hospitals.
    B) eliminate all possible noncardiac diagnoses before proceeding.
    C) avoid unnecessary treatment for persons low at risk for significant CAD.
    D) provide immediate information about coronary vessels and extent of atherosclerosis.

    TREATMENT OF UA/NSTEMI

    The objective of an ischemia-guided strategy is to avoid unnecessary treatment (and associated costs) for patients at low risk for significant CHD. The ACC/AHA guideline notes that an ischemia-guided strategy may be considered for patients with NSTE-ACS who are initially stabilized and at elevated risk for clinical events (class IIbB) [3]. It is also reasonable to consider clinician and patient preference in decision making about an ischemia-guided strategy (class IIbC). Patients at low or intermediate risk who have had no ischemia at rest or with low-level activity for at least 12 to 24 hours should have noninvasive stress testing (class IB) [3].

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    21 . Of the following, which medication is prescribed in variant angina to prevent coronary vasospasm?
    A) Diltiazem
    B) Metoprolol
    C) Simvastatin
    D) Amiodarone

    TREATMENT OF UA/NSTEMI

    The primary medical therapy for management of variant or vasospastic angina involves nitrates and calcium-channel blockers. Within minutes of administration, nitroglycerin has been found to effectively treat episodes of angina and myocardial ischemia caused by vasospasm. Long-acting nitrates can reduce the frequency of recurrent episodes of chest pain. Calcium-channel blockers, specifically nifedipine, amlodipine, verapamil, and diltiazem, are prescribed to prevent coronary vasospasm and the subsequent ischemia that can result. In this patient population, calcium-channel blockers are preferred over beta blockers [213,214].

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    22 . Of the following, which class of medications may be used to manage neuropsychiatric symptoms of cocaine-induced ACS?
    A) Antiplatelets
    B) Anticoagulants
    C) Benzodiazepines
    D) Glycoprotein IIb/IIIa inhibitors

    MANAGEMENT OF COCAINE-INDUCED ACS

    Patients with cocaine-induced chest pain who show ECG and biomarker evidence of ischemia or infarct should be admitted for monitoring, observation, and further treatment as indicated. General medical therapies, similar to those used in management of non-cocaine related ACS, should be employed. In addition, the use of IV benzodiazepines as part of the early management of these patients may be indicated. In patients who use cocaine, benzodiazepines help to relieve chest pain and manage neuropsychiatric manifestations. Aspirin, calcium-channel blockers, and nitroglycerin are also recommended; beta blockers are not recommended with acute cocaine intoxication [3,48,215].

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    23 . Preferred treatment for STEMI is
    A) CABG.
    B) rescue PCI.
    C) primary PCI.
    D) fibrinolytic therapy.

    TREATMENT OF STEMI

    Reperfusion therapy is the cornerstone in the management of STEMI, and antiplatelet and anticoagulant agents are necessary as ancillary therapy. The options for reperfusion include revascularization procedures and/or pharmacologic (fibrinolytic) therapy. As with the treatment for NSTEMI, the use of PCI has become the primary approach to revascularization; approximately 80% to 90% of patients have PCI revascularization based on angiographic findings [218]. In addition, PCI is the preferred strategy for reperfusion because of its superior outcomes compared with fibrinolytic therapy [2,218]. However, gaining the optimal benefit from PCI depends on many factors, and timing is the most important variable in selecting a reperfusion therapy [2,216]. Care should also be taken to evaluate patients for contraindications to fibrinolytic therapy [5].

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    24 . For PCI in STEMI, the targeted door-to-device time is within less than
    A) 10 minutes from onset of symptoms.
    B) 30 minutes from initial diagnostic ECG.
    C) 90 minutes from time of patient's arrival at the emergency department.
    D) 2 hours from time of initial chest pain.

    TREATMENT OF STEMI

    The 2013 ACCF/AHA guideline indicates that PCI is preferred over fibrinolytic therapy for patients with STEMI when it can be performed in a timely manner by experienced operators [2]. PCI should be done within less than 90 minutes after the patient's arrival at the emergency department (door-to-device time) [2]. If PCI cannot be done within 90 minutes, fibrinolytic therapy should be initiated as the reperfusion strategy within 120 minutes of the first medical contact

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    25 . One strategy to improve timely reperfusion therapy in STEMI is
    A) decreased use of fibrinolytics.
    B) EMS use of pre-hospital ECGs.
    C) creation of ECG banks to store data.
    D) increased facility-to-facility transport of patients.

    TREATMENT OF STEMI

    Specific strategies that have improved the door-to-device time interval focus on three key components: door-to-ECG time, ECG-to-catheterization laboratory time, and laboratory arrival-to-device time. The ACCF/AHA provides the following steps as a general protocol in improving door-to-device times [2]:

    • A prehospital ECG to diagnose STEMI is used to activate the PCI team while the patient is en route to the hospital.

    • Emergency physicians activate the PCI team.

    • A single call to a central page operator activates the PCI team.

    • A goal is set for the PCI team to arrive in the catheterization laboratory within 20 minutes after being paged.

    • Timely data feedback and analysis are provided to members of the STEMI care team.

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    26 . Which of the following is an early sign of a retroperitoneal bleed following PCI?
    A) Pallor
    B) Constipation
    C) Severe flank pain
    D) Reduction in elevated biomarkers

    TREATMENT OF STEMI

    Bleeding may occur from the arterial puncture site. Initial indications include frank bleeding from the puncture site and/or development of a hematoma in the area surrounding the site. A retroperitoneal bleed may also occur; an early sign is a complaint of severe flank pain. To reduce the likelihood of bleeding, the patient should be maintained on bed rest as specified by physician orders. The length of time bed rest is indicated depends on the method used to close the arterial puncture site. The arterial puncture site, often the femoral artery, should be monitored frequently for signs of bleeding or hematoma formation [33,224].

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    27 . An allergy or intolerance to infusing glycoprotein IIb/IIIa inhibitors may cause
    A) stent occlusion.
    B) increased clotting.
    C) elevated hemoglobin.
    D) a significant drop in platelet count.

    TREATMENT OF STEMI

    A significant drop in platelet count may be caused by an allergy or intolerance to infusing glycoprotein IIb/IIIa inhibitors. With a drop in platelet count, the patient's risk of bleeding increases. Patients receiving glycoprotein IIb/IIIa inhibitors should have a complete blood count checked at designated intervals to make sure that platelet counts are not dropping. Parameters should include orders to notify the physician if the platelet count drops below a specified level. If a patient develops a significant drop in platelet count, the infusion of the glycoprotein IIb/IIIa inhibitor is discontinued and the patient is placed on bleeding precautions and observed carefully for any signs of bleeding [33,224].

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    28 . Fibrinolytic therapy should be given to patients with STEMI who have no contraindications and onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary PCI cannot be performed within of how many minutes of first medical contact?
    A) 30 minutes
    B) 60 minutes
    C) 120 minutes
    D) 180 minutes

    TREATMENT OF STEMI

    Although the focus of treatment for patients presenting with STEMI is often given to PCI, fibrinolytic therapy is the treatment of choice for some patients. If a patient arrives at or is transported by EMS to a non-PCI-capable facility, the decision whether to immediately transfer to a PCI-capable facility or administer fibrinolytic therapy must be made. Factors that affect this decision include the time from onset of symptoms, the risk of complications related to STEMI, the risk of bleeding with fibrinolysis, the presence of shock or severe heart failure, and the time required for transfer to a PCI-capable hospital. The ACCF/AHA guideline recommends that, in the absence of contraindications, fibrinolytic therapy should be given to patients with STEMI and onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary PCI cannot be performed within 120 minutes of first medical contact [2].

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    29 . Which of the following is an absolute contraindication to fibrinolytic therapy?
    A) Pregnancy
    B) Severe hypotension
    C) History of peptic ulcer
    D) Prior intracranial hemorrhage

    TREATMENT OF STEMI

    CONTRAINDICATIONS AND CAUTIONS FOR FIBRINOLYSIS USE IN ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)a

    Absolute Contraindications
    Any prior intracranial hemorrhage
    Known structural cerebral vascular lesion (e.g., arteriovenous malformation)
    Known malignant intracranial neoplasm (primary or metastatic)
    Ischemic stroke within three months EXCEPT acute ischemic stroke within 4.5 hours
    Suspected aortic dissection
    Active bleeding or bleeding diathesis (excluding menses)
    Significant closed-head or facial trauma within three months
    Intracranial or intraspinal surgery within two months
    Severe uncontrolled hypertension (unresponsive to emergency therapy)
    For streptokinase, prior treatment within the previous six months
    Relative Contraindications
    History of chronic, severe, poorly controlled hypertension
    Substantial hypertension on presentation (systolic greater than 180 mm Hg or diastolic greater than 110 mm Hg)
    History of prior ischemic stroke (greater than three months)
    Dementia
    Known intracranial pathology not covered in absolute contraindications
    Traumatic or prolonged (greater than 10 minutes) CPR
    Major surgery (within less than three weeks)
    Recent (within two to four weeks) internal bleeding
    Noncompressible vascular punctures
    Pregnancy
    Active peptic ulcer
    Oral anticoagulant therapy
    aViewed as advisory for clinical decision making and may not be all-inclusive or definitive.
    INR = international normalization ratio; CPR = cardiopulmonary resuscitation.
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    30 . Nursing assessment after fibrinolytic therapy should include
    A) continuous ECG monitoring.
    B) frequent vital sign monitoring.
    C) assessment for recurrence of chest pain.
    D) All of the above

    TREATMENT OF STEMI

    Immediately following reperfusion with fibrinolytics, the patient is at risk to develop serious bleeding episodes or to reocclude the infarct-related vessel [33,220]. Nursing assessment during this period is crucial and should include [33]:

    • Continuous ECG monitoring for rate, rhythm, or reoccurrence of signs of acute ischemia, development of life-threatening arrhythmias

    • Assessment for reoccurrence of chest pain or other symptoms associated with an acute ischemic episode

    • Frequent vital sign monitoring for hypotension, drop in oxygen saturation, or other signs indicative of developing heart failure

    • Assessment for any changes in level of consciousness

    • Assessment for indications of bleeding

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    31 . The drug of choice to manage pain associated with STEMI is
    A) aspirin.
    B) ticlopidine.
    C) an NSAID.
    D) IV morphine sulfate.

    TREATMENT OF STEMI

    The drug of choice to manage the pain associated with STEMI is intravenous morphine sulfate [2]. Morphine sulphate is indicated to relieve ongoing ischemic discomfort, control hypertension, ameliorate anxiety, or manage pulmonary edema. The initial dose should be 4–8 mg, with lower doses in the elderly. Additional doses of 2–8 mg may be given at intervals of 5 to 15 minutes [2].

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    32 . Of the following medications, which is strongly recommended for patients recovering from STEMI and an acute anterior infarction or pulmonary congestion?
    A) Amiodarone
    B) ACE inhibitor
    C) Benzodiazepine
    D) COX-2 inhibitor

    TREATMENT OF STEMI

    The use of an oral ACE inhibitor is a strong recommendation for all patients recovering from STEMI, including those with anterior infarction, pulmonary congestion, or LVEF of less than 0.40, as well as those with normal LVEF in whom cardiovascular risk factors are well controlled [2]. Adherence to this recommendation has increased since the late 1990s but remains low [203,250,251,252]. In addition, the doses used in clinical practice have been lower than the target doses used in clinical trials [252].

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    33 . Which of the following statements regarding calcium-channel blockers is TRUE?
    A) Verapamil should be used for patients with heart failure.
    B) Nifedipine should be incorporated into the treatment of STEMI.
    C) Diltiazem should be used for patients with left ventricular dysfunction.
    D) Early treatment with dihydropyridine calcium antagonists has not been found to improve rates of mortality or reinfarction.

    TREATMENT OF STEMI

    Early treatment with dihydropyridine calcium antagonists (nifedipine and nicardipine) has not been found to improve rates of mortality or reinfarction [2]. Nifedipine is contraindicated in the treatment of STEMI. Although verapamil and diltiazem may be useful to relieve ongoing or recurrent ischemia, lower blood pressure, or control the ventricular response rate to atrial fibrillation when beta blockers are contraindicated (and the patient has well-preserved left ventricular function and no clinical evidence of congestive heart failure or pulmonary congestion), no specific recommendation for their use exists in the 2013 STEMI guideline [2,3]. Both drugs have been associated with significantly reduced mortality and major cardiovascular events [256,257]. Verapamil should not be used for patients with heart failure or bradyarrhythmias, and diltiazem should not be used for patients with left ventricular dysfunction [2].

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    34 . Healthcare providers can help to improve adherence to smoking cessation by
    A) recommending the use of smokeless tobacco.
    B) allowing support groups and peer counselors to take sole responsibility.
    C) engaging in repeated contacts during the hospital stay and beyond three months.
    D) All of the above

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    Quitting smoking has been described as "probably the most important thing a smoker with acute MI can do to improve future health" [261]. Mortality after an ACS event for a patient who smokes cigarettes is twice that for a patient who does not, but cessation of smoking reduces reinfarction and death rates at one year [2]. Clinicians should use the in-hospital period after MI and each office visit as an opportunity to ask patients who were smokers if they have quit or are ready to quit and should offer counseling, pharmacologic support, and information on formal quit programs. The in-hospital period is unique because many patients are motivated to quit and are typically unable to smoke for three to nine days. Randomized controlled trials have shown that repeated contacts during the hospital stay and at and beyond three months (typically by telephone) are more likely to result in smoking cessation [2]. A Cochrane review showed that only intensive counseling programs work and that nicotine replacement further increases the rates of successful cessation among patients in intensive programs [262]. Another Cochrane review found high-quality evidence for a benefit of combined pharmacotherapy (with any type of nicotine-replacement therapy, bupropion, nortriptyline, or varenicline) and behavioral treatment compared with usual care, brief advice, or less intensive behavioral support [263]. However, many clinicians are reluctant to add another drug to the multitude of medications prescribed after MI.

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    35 . What is the goal body mass index for patients after ACS?
    A) Less than 18.5
    B) 18.5–24.9
    C) 22.5–29
    D) 25–30

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    Obesity is another well-documented risk factor for CHD, and weight management programs and information on healthy eating/caloric intake should be promoted as appropriate [260]. The patient's body mass index and waist circumference should be measured at each visit. The goal is to attain a body mass index of 18.5–24.9 and a waist circumference of 35 inches (women) or 40 inches (men) [260]. When weight reduction is needed, the initial goal is weight loss of 5% to 10% from baseline [260].

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    36 . Following hospitalization for ACS, what is the recommended antiplatelet therapy after discharge?
    A) Lovastatin
    B) Metoprolol
    C) Enoxaparin
    D) Low-dose aspirin and a P2Y12 inhibitor

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    The recommended antiplatelet therapy after discharge is a combination of aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) [2,146,260]. The findings of studies have suggested that low-dose aspirin is as effective as higher doses but has a better safety profile [179,235,265]. The recommended daily dose of aspirin is 75–162 mg for all patients, and the ACC/AHA guidelines for the management of STEMI and NSTE-ACS state that it is reasonable to a use an 81-mg dose [2,3,146,235]. However, despite the better safety profile of low-dose aspirin, data have indicated that 325 mg is the most common dose, prescribed for 55.7% of patients with UA/NSTEMI [266].

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    37 . What is the recommended antithrombotic agent for patients with UA/NSTEMI or STEMI?
    A) Warfarin
    B) Diltiazem
    C) Abciximab
    D) Beta blockers and ACE inhibitors

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    Questions about clopidogrel maintenance therapy remain, as the optimal dose and duration of therapy have not been identified [146,182,267,268]. Another concern is the effect of stopping clopidogrel. In a 2008 study of 3,137 patients with ACS (treated either medically or with PCI) who took clopidogrel for a mean of 9 to 10 months, there was a significantly high risk of adverse events in the initial 90 days after stopping treatment with clopidogrel [269]. The reason for this phenomenon is unclear, and the authors suggested that strategies to reduce the incidence of such early events should be identified [269]. Additionally, the response to clopidogrel varies among patients, and diminished responsiveness has been observed [146]. A 2010 retrospective study of 2,017 patients with ACS, conducted to confirm the findings of the 2008 study, found that the 0- to 90-day interval after stopping clopidogrel was associated with higher risk of death/MI compared with the 91- to 360-day interval. There was a similar trend of increased adverse events 0 to 90 days after stopping clopidogrel for various subgroups (i.e., women versus men, medical therapy versus PCI, stent type, and ≥6 months or <6 months of clopidogrel treatment) [270]. Warfarin is recommended as an antithrombotic for patients with UA/NSTEMI or STEMI who are allergic to aspirin [146,260].

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    38 . The target level for LDL-C with statin therapy in average-risk patients is
    A) less than 100 mg/dL.
    B) 200–225 mg/dL.
    C) 250–300 mg/dL.
    D) greater than 400 mg/dL.

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    The goal of statin therapy is to achieve an LDL level less than 100 mg/dL for patients with average risk, and an LDL level of less than 70 mg/dL is reasonable for very-high-risk patients [2]. If the triglyceride level is 200 mg/dL or higher, the non-HDL cholesterol should be less than 130 mg/dL in patients with average risk, whereas a non-HDL cholesterol level of less than 100 mg/dL is reasonable for very-high-risk patients. Statin therapy should be supplemented with dietary modification, weight management, and exercise. Patients should be encouraged to follow a diet with an increase of fresh fruits and vegetables, with less than 7% of total calories as saturated fat, less than 1% of total calories as trans fatty acids, and less than 200 mg per day of cholesterol [2,260].

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    39 . Treatment for hypertension is recommended when greater than
    A) 120–129/80 mm Hg.
    B) 130/80 mm Hg.
    C) 140/90 mm Hg.
    D) 150/90 mm Hg.

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    In addition, blood pressure should be controlled according to the 2017 Guideline for High Blood Pressure in Adults, which recommends treatment when blood pressure is elevated, defined as 120–129/<80 mm Hg [67]. The guideline recommends initial treatment with nonpharmacologic interventions and lifestyle changes. Initiation of pharmacologic treatment is recommended for secondary prevention in patients with clinical CVD and an average systolic blood pressure of 130 mm Hg or greater or an average diastolic blood pressure of 80 mm Hg or greater and for primary prevention in adults with an estimated 10-year atherosclerotic cardiovascular disease risk of 10% or higher and an average systolic blood pressure of 130 mm Hg or greater or an average diastolic blood pressure of 80 mm Hg or greater [67]. The AHA/ACCF recommends initial treatment with a beta blocker and/or an ACE inhibitor as secondary prevention for patients with CHD [260].

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    40 . Which of the following issues negatively impacts patients' adherence to medication therapy?
    A) Higher education level
    B) High number of medications
    C) Having transportation to a pharmacy
    D) Lower number of prescribed medications

    DISCHARGE PLANNING AND SECONDARY PREVENTION

    Lack of patient compliance with medications is also a serious problem and has been referred to as an unrecognized risk factor for CHD, because of its association with significant increases in adverse events and health costs [295,296]. Among individuals with CHD (many of whom had experienced a recent ACS event), compliance with guideline-recommended medications has ranged from 18% to 55%. Approximately 54% of individuals have been compliant with all of their initial medications, and compliance decreases over time [296,297,298]. One study showed that compliance was 60.3% at one year, 53.7% at two years, and 48.8% at five years [299]. Individuals who discontinue medications are more likely to be older, female, unmarried, and less educated [298]. Several other factors have been found to be associated with noncompliance with medications [296,297,298]:

    • Choice of medication

    • Tolerability

    • Duration of treatment

    • Dosing frequency

    • Higher number of prescribed medications

    • Lack of symptoms as indication for the medication

    • Uncertainty about how to take the medication

    • Lack of transportation to the pharmacy

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